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Naïve and LCMV Cl13 infected liver tissue of ERT2 AlbCre Ifnar1 fl/fl mice

ABSTRACT: Naïve and LCMV Cl13 infected liver tissue of ERT2 AlbCre Ifnar1 fl/fl mice

PROVIDER: PRJNA481515 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9150100.fastq.gz	Fastqsanger.gz
	SRR9150101.fastq.gz	Fastqsanger.gz
	SRR9150092.fastq.gz	Fastqsanger.gz
	SRR9150102.fastq.gz	Fastqsanger.gz
	SRR9150093.fastq.gz	Fastqsanger.gz

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Naïve and LCMV Cl13 infected liver tissue of ERT2 AlbCre Ifnar1 fl/fl mice

Project description:Age- and sex-matched (male, 2-3 months old) ERT2 AlbCre Ifnar fl/fl and ERT2 AlbCre Ifnar +/+ mice were injected intraperitoneally with 40 mg/kg tamoxifen for 5 consective days. Mice were then intravenously infected with 2x10^6 focus forming units of LCMV Cl13 and liver tissue of either genotype was harvested 1.5 days post infection and analyzed for transcriptomic changes (n = 3). Liver tissue of uninfected animals of both genotypes was harvested as control (n = 3).

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Project description:To evaluate the potential role of Hes1 in regulation of type I IFNs and the downstream ISGs expression, we generated the bone marrow-derived macrophages (BMDMs) from Hes1+/+ Cre-ERT2 and Hes1fl/fl Cre-ERT2 mice. RNA-sequencing analysis of Poly(I:C) [(polyinosinic: polycytidylic acid), a mimic of viral double-stranded RNA]-treated BMDMs revealed that 49 genes were induced more than two-fold by Poly(I:C) for 3 hrs in Hes1-deficient BMDMs relative to their expression in Hes1+/+Cre-ERT2 cells. Notably, 67.3% of these upregulated genes were ISGs by screening the Interferome database, suggesting that Hes1 inhibits expression of TLR-mediated ISGs,these results indicated that Hes1 negatively regulates TLR3-mediated induction of ISGs in macrophages.

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Project description:Inhibition of IFN-I signaling promotes the control of persistent virus infection, but the underlying mechanisms remain poorly understood. Here we report that genetic ablation of IFNAR1 specifically in NK cells led to elevated numbers of T follicular helper cells, germinal center B cells, and plasma cells, resulting in hastened virus clearance comparable to IFNAR1 blockade by an IFNAR1 neutralizing antibody. Antigen-specific B cells and antiviral antibodies were essential for the accelerated control of LCMV Cl13 infection following IFNAR1 blockade. IFNAR1 signaling in NK cells promoted NK cell maturation, function, and killing of antigenspecific CD4 and CD8 T cells. Therefore, Inhibition of IFN I signaling in NK cells enhances CD4 and CD8 T cell responses, elevates humoral immune response, and thereby facilitates the control of persistent virus infection.

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